UVB-mediated induction of cytokines and growth factors in pterygium epithelial cells involves cell surface receptors and intracellular signaling.

摘要: Purpose Pterygium is a proliferative, inflammatory, and invasive ocular surface disease associated with excessive ultraviolet (UV) exposure. This investigation was conducted to identify UV activated signaling pathways in pterygium epithelial cells (PECs) that mediate cytokine growth factor production determine whether these are sensitive blockade by anti-inflammatory agents such as retinoic acid (RA) interferon (IFN)-alpha. Methods PECs were pretreated or without inhibitors of the ERK1/2, JNK, p38 (PD98059, SB202190, SB203580, respectively) mitogen-activated protein kinases (MAPK) tyrosine kinase activity epidermal receptor (EGFR; PD153035) platelet-derived (PDGF; AG1295); exposed UVB (20 mJ/cm2); then further treated same inhibitors. Media harvested analyzed ELISA for interleukin (IL)-6, IL-8, vascular endothelial (VEGF). Cytokine mRNA assessed reverse transcription-polymerase chain reaction (RT-PCR). Results Inhibitors MAPKs significantly abolished UVB-mediated increase IL-6, VEGF. PD153035 reduced AG1295 repressed both partially downregulated VEGF UV-exposed PECs. RA IFN-alpha dose dependently abrogated IL-6 IL-8 but had no effect on expression after Conclusions The results have identified stress-induced intracellular pathway potential cell-surface transmitters may be relevant development. Moreover, two anti-inflammatory/antiangiogenic study model. Topical application drugs benefit patients pterygia, potentially reducing necessity surgical intervention.